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七叶皂苷对牙龈卟啉单胞菌衍生脂多糖诱导的SH-SY5Y细胞损伤的抗凋亡作用

Anti-Apoptotic Effects of Escin on Porphyromonas gingivalis-Derived Lipopolysaccharide-Induced Injury in SH-SY5Y Cells.

作者信息

Sun Yingying, Zhang Rui, Pan Yunping, Sun Yufei, Liu Limin, Feng Min, Du Yuan, Wang Tian, Liu Shutai

机构信息

Department of Periodontology, Shenzhen Stomatology Hospital, Shenzhen, Guangdong, China.

Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, School of Pharmacy, Yantai University, Yantai, Shandong, China.

出版信息

Brain Behav. 2025 Sep;15(9):e70810. doi: 10.1002/brb3.70810.

DOI:10.1002/brb3.70810
PMID:40891167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12402593/
Abstract

BACKGROUND

Porphyromonas gingivalis-derived lipopolysaccharide (Pg-LPS) may be associated with the pathogenesis of Parkinson's disease and other neurodegenerative disorders. Escin is a bioactive compound found in the horse chestnut tree (Aesculus hippocastanum). This research investigated the impact of escin on Pg-LPS-induced injury in SH-SY5Y cells.

METHODS

Parkinson's disease model was established using SH-SY5Y neuronal cells. Cell viability was evaluated with MTT assays. Cell morphology was observed by fluorescence microscopy. Apoptosis was detected by JC-1, TUNEL, and Hoechst/propidium iodide staining, and flow cytometric analysis. The mRNA levels of BCL2 and BAX were determined by RT-PCR, and the protein levels of BCL2/BAX, cleaved Caspase 3/Caspase 3, and PARP were evaluated through Western blotting.

RESULTS

Escin mitigated the reduction in viability of SH-SY5Y cells caused by Pg-LPS. Pg-LPS triggered apoptosis in SH-SY5Y cells, alleviated by escin dose-dependently. Furthermore, the anti-apoptotic effect of escin was reversed by a specific apoptotic inducer.

CONCLUSIONS

Pg-LPS leads to SH-SY5Y cells' mitochondria malfunction and programed cell death. Escin alleviated SH-SY5Y cell injury induced by Pg-LPS through its anti-apoptotic effects.

摘要

背景

牙龈卟啉单胞菌衍生的脂多糖(Pg-LPS)可能与帕金森病及其他神经退行性疾病的发病机制有关。七叶皂苷是在七叶树(欧洲七叶树)中发现的一种生物活性化合物。本研究调查了七叶皂苷对Pg-LPS诱导的SH-SY5Y细胞损伤的影响。

方法

利用SH-SY5Y神经元细胞建立帕金森病模型。通过MTT法评估细胞活力。通过荧光显微镜观察细胞形态。通过JC-1、TUNEL和Hoechst/碘化丙啶染色以及流式细胞术分析检测细胞凋亡。通过RT-PCR测定BCL2和BAX的mRNA水平,并通过蛋白质印迹法评估BCL2/BAX、裂解的半胱天冬酶3/半胱天冬酶3和PARP的蛋白质水平。

结果

七叶皂苷减轻了Pg-LPS引起的SH-SY5Y细胞活力降低。Pg-LPS诱导SH-SY5Y细胞凋亡,七叶皂苷呈剂量依赖性减轻凋亡。此外,七叶皂苷的抗凋亡作用被一种特异性凋亡诱导剂逆转。

结论

Pg-LPS导致SH-SY5Y细胞线粒体功能障碍和程序性细胞死亡。七叶皂苷通过其抗凋亡作用减轻了Pg-LPS诱导的SH-SY5Y细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/7bac5b036587/BRB3-15-e70810-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/6614f41f7d12/BRB3-15-e70810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/4ec4aa046912/BRB3-15-e70810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/3eece3b129ff/BRB3-15-e70810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/cf3e8eb7d930/BRB3-15-e70810-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/8dafdb4a2168/BRB3-15-e70810-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/7bac5b036587/BRB3-15-e70810-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/6614f41f7d12/BRB3-15-e70810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/4ec4aa046912/BRB3-15-e70810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/3eece3b129ff/BRB3-15-e70810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/cf3e8eb7d930/BRB3-15-e70810-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/8dafdb4a2168/BRB3-15-e70810-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09fa/12402593/7bac5b036587/BRB3-15-e70810-g005.jpg

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本文引用的文献

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J Periodontal Res. 2025 May 9. doi: 10.1111/jre.13416.
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Escin Rescues Blood-brain Barrier and Inhibits NLRP3 Inflammasome-mediated Pyroptosis in Rats with Superior Sagital Sinus Thrombosis.七叶皂苷钠对大鼠上矢状窦血栓形成模型血脑屏障的保护作用及对NLRP3炎性小体介导的细胞焦亡的抑制作用
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Chronic Oral Inoculation of Porphyromonas gingivalis and Treponema denticola Induce Different Brain Pathologies in a Mouse Model of Alzheimer Disease.
慢性口服牙龈卟啉单胞菌和密螺旋体感染诱导阿尔茨海默病小鼠模型的不同脑病理学改变。
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Classical apoptotic stimulus, staurosporine, induces lytic inflammatory cell death, PANoptosis.经典凋亡刺激物,星形孢菌素,诱导裂解炎症细胞死亡,即 PANoptosis。
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LRRK2 regulates ferroptosis through the system Xc-GSH-GPX4 pathway in the neuroinflammatory mechanism of Parkinson's disease.LRRK2 通过帕金森病神经炎症机制中的系统 Xc-GSH-GPX4 通路调控铁死亡。
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